Abstract:
:Active variant surface glycoprotein (VSG) gene chromatin is preferentially digested by the restriction enzyme HinfI in nuclei of bloodstream variants of Trypanosoma brucei. HinfI sensitivity of VSG gene chromatin is not observed in nuclei of relapse variants in which the VSG gene has been inactivated in situ. Active VSG gene chromatin is preferentially degraded by the single-strand-specific endonucleases S1 and Bal31. This sensitivity is not the result of pre-existing single-strand breaks or a detectably altered nucleosomal organization. Trypanosome nuclei in which the run-on transcription of VSG genes has been specifically shut down have been used to show that Hinfl and Bal31 sensitivity is not dependent upon continued transcription of the VSG gene. The presence of single-stranded DNA regions within VSG gene chromatin is consistent with a model in which VSG genes are activated by increased torsional stress.
journal_name
J Mol Bioljournal_title
Journal of molecular biologyauthors
Greaves DR,Borst Pdoi
10.1016/0022-2836(87)90559-6subject
Has Abstractpub_date
1987-10-05 00:00:00pages
471-83issue
3eissn
0022-2836issn
1089-8638pii
0022-2836(87)90559-6journal_volume
197pub_type
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